Nephrology (Carlton, Vic.)最新文献

{"title":"Correction to \"Finerenone Attenuates Peritoneal Fibrosis by Restoring Autophagy Flux\".","authors":"","doi":"10.1111/nep.70243","DOIUrl":"10.1111/nep.70243","url":null,"abstract":"","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70243"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148407861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Antiresorptive Treatment on Bone Mineral Density and Bone Turnover Markers in a Child With Steroid-Resistant Nephrotic Syndrome: A Case Report.","authors":"Jun Aoyagi, Takahiro Kanai, Takane Ito, Masanori Kurosaki, Tomomi Maru, Marika Ishii, Kazuya Tanimoto, Toshihiro Tajima","doi":"10.1111/nep.70245","DOIUrl":"10.1111/nep.70245","url":null,"abstract":"<p><p>Glucocorticoid-induced osteoporosis (GIOP) is a significant complication of prolonged glucocorticoid treatment in paediatric nephrotic syndrome, but the optimal treatment strategy remains unclear. We report the case of a 17-year-old boy with steroid-resistant nephrotic syndrome due to focal segmental glomerulosclerosis who developed progressive bone fragility during high-dose glucocorticoid treatment. Four months after initiation of glucocorticoids, his lumbar bone mineral density (BMD) decreased 9.2%, serum alkaline phosphatase (S-ALP) decreased 22% and serum tartrate-resistant acid phosphatase-5b (S-TRACP-5b) increased 47% compared with baseline, indicating compromised bone strength. Oral alendronate (35 mg/week) was initiated to prevent progression of GIOP. One month after antiresorptive treatment, S-TRACP-5b decreased 87% from the level measured at 4 months. BMD and S-ALP initially continued to decline slightly until 7 months but subsequently demonstrated sustained recovery. S-TRACP-5b levels were lower than baseline levels to a greater extent than the S-ALP levels between 5 and 28M, corresponding to progressive improvement in the BMD. No fragility fractures or adverse events occurred, and remission of nephrotic syndrome was maintained. This case suggests that alendronate rapidly suppresses bone resorption, promotes a bone formation-dominant state in conjunction with glucocorticoid tapering and may prevent bone fragility in paediatric GIOP. A ≥ 34% increase in S-TRACP-5b accompanied by a ≥ 22% decrease in S-ALP from baseline may indicate the appropriate timing for initiating antiresorptive treatment. Further investigations are warranted to establish evidence-based management strategies for paediatric GIOP.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70245"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148400475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paroxysmal Cold Haemoglobinuria: A Chilling Case of Acute Renal Failure.","authors":"Alastair Weng, Samantha Gardiner, Aspasia Pefanis, Shirlene Sim","doi":"10.1111/nep.70241","DOIUrl":"10.1111/nep.70241","url":null,"abstract":"<p><p>We describe a rare case of a 64-year-old man with acute renal failure secondary to paroxysmal cold haemoglobinuria (PCH), presenting with haemoglobinuria, jaundice, and fevers. PCH is an intravascular haemolytic anaemia with polyphasic IgG antibody binding of red blood cells at cold temperatures, with complement-mediated haemolysis on rewarming. Renal biopsy confirmed acute tubular necrosis without thrombotic microangiopathy. The patient received supportive management including intermittent haemodialysis with a warm circuit to prevent further haemolysis and achieved full renal recovery. Optimal therapy of PCH varies in the literature.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70241"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148364759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of Electronic Health Data-Based Frailty Assessment Tools for Prediction of Adverse Outcomes of Patients With Chronic Kidney Disease.","authors":"Ying Deng, Jianhao Kang, Xinghua Guo, Shaomin Li, Hualiang Liang, Leile Tang, Xun Liu","doi":"10.1111/nep.70232","DOIUrl":"10.1111/nep.70232","url":null,"abstract":"<p><strong>Aim: </strong>To compare four electronic health record (EHR)-based frailty tools-the Hospital Frailty Risk Score (HFRS), Johns Hopkins Adjusted Clinical Groups Frailty Indicator (CFI), Electronic Frailty Index (eFI) and a Laboratory-based Frailty Index (FI-Lab)-in predicting progression and all-cause mortality in hospitalised patients with chronic kidney disease (CKD).</p><p><strong>Methods: </strong>This retrospective study evaluated the indices in two cohorts: a single-centre cohort (n = 5715) for CKD progression and the Medical Information Mart for Intensive Care (MIMIC) database (n = 2674) for mortality. We used Cox proportional hazards regression for association analyses. The incremental predictive value of adding frailty indices to established risk models was quantified using the area under the curve (AUC), net reclassification improvement (NRI) and integrated discrimination improvement (IDI).</p><p><strong>Results: </strong>Correlations between the frailty indices were weak to moderate (Spearman's ρ = 0.205-0.451). In adjusted analyses, CFI, eFI and FI-Lab were associated with a higher risk of CKD progression, whereas HFRS was not. In the MIMIC cohort, all four indices were significantly associated with all-cause mortality. Notably, the CFI association was non-significant in patients < 65 years for both CKD progression and 28-day mortality. For predictive enhancement, adding FI-Lab and eFI to established CKD risk models significantly improved progression prediction (ΔAUC p < 0.05), yielding substantial reclassification (NRI: 0.376-0.498) and discrimination (IDI: 0.032-0.048). For mortality prediction, all indices improved baseline severity scores, with FI-Lab providing the greatest incremental value.</p><p><strong>Conclusion: </strong>Among the evaluated EHR-based frailty indices, FI-Lab offers the most robust utility for risk stratification in hospitalised patients with CKD, followed closely by eFI.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 7","pages":"e70232"},"PeriodicalIF":1.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13371995/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148451337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kidney Health for All: Caring for People, Protecting the Planet.","authors":"Raymond Vanholder, Dina Abdellatif, Augusto Cesar Soares Dos Santos, Ricardo Correa-Rotter, Natarajan Gopalakrishnan, Bill Wang, Stefanos Roumeliotis, Alessandro Balducci, Ágnes Haris, Manjusha Yadla, Li-Li Hsiao","doi":"10.1111/nep.70230","DOIUrl":"10.1111/nep.70230","url":null,"abstract":"<p><p>The current kidney care model-focused on late-stage disease and in-center haemodialysis-is unsustainable because of costs, environmental burden, poor outcomes, and reduced quality of life. The 78th World Health Assembly's recognition of kidney disease as a serious health threat presents a critical opportunity to reshape kidney care. Aligned with this, the 2026 World Kidney Day theme, \"Kidney Health for All: Caring for People, Protecting the Planet\", calls for a systematic change. A sustainable model must prioritize early detection and prevention, reducing the need for kidney replacement therapy. Transplantation and home dialysis benefit people with kidney failure, environment and society. Dialysis itself must become more eco-friendly without compromising care quality, recognizing that planetary perturbations in turn affect kidney health. Conservative care should also be considered, particularly for elderly and frail patients, if the quality-of-life benefits outweigh the perspectives offered by dialysis. Achieving this shift requires coordinated action across all stakeholders: education and engagement of the public, policy makers and health professionals to raise awareness about the threat of kidney disease; and an urgent move toward patient-centered care.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70230"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148207587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NCOA4-Mediated Ferroptosis Drives Tubulointerstitial Fibrosis in Hyperuricemia-Associated Chronic Kidney Disease.","authors":"Minhui Wang, Ying Zhang, Daojun Chen, Jiali Wei","doi":"10.1111/nep.70228","DOIUrl":"https://doi.org/10.1111/nep.70228","url":null,"abstract":"<p><strong>Aim: </strong>This study aimed to elucidate whether NCOA4-mediated ferritinophagy promotes ferroptosis and contributes to renal tubulointerstitial fibrosis, and to clarify its interaction with the Nrf2 antioxidant pathway.</p><p><strong>Methods: </strong>A uric acid (UA)-induced ferroptosis model was established in HK-2 cells and a hyperuricemic nephropathy (HN) model was constructed in C57BL/6 mice using adenine and potassium oxonate gavage. NCOA4 and Nrf2 were silenced by shRNA in vitro and AAV9-mediated knockdown in vivo. Ferroptosis, oxidative stress and fibrosis were evaluated using qRT-PCR, western blotting, immunofluorescence, biochemical assays and histopathological staining.</p><p><strong>Results: </strong>UA exposure significantly increased NCOA4 expression, promoted ferritin degradation, and triggered iron accumulation, lipid peroxidation, and suppression of the Nrf2/GPX4/SLC7A11 axis. NCOA4 knockdown increased antioxidant defences, reduced Fe²⁺ and ROS levels and alleviated α-SMA and collagen IV expression in both HK-2 cells and HN mice. However, co-silencing Nrf2 abolished these protective effects, indicating functional coupling between NCOA4 and Nrf2 signalling.</p><p><strong>Conclusion: </strong>NCOA4-mediated ferritinophagy acts as an upstream driver of ferroptosis and tubulointerstitial fibrosis in hyperuricemia-associated CKD. The NCOA4/Nrf2 axis represents a mechanistic link and potential therapeutic target for preventing renal fibrosis.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70228"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148298562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on 'Chronic Kidney Disease-Associated Pruritus in Patients on Home Haemodialysis'.","authors":"Madhuri Tribhuvan, Shashikant N Phatke","doi":"10.1111/nep.70236","DOIUrl":"https://doi.org/10.1111/nep.70236","url":null,"abstract":"","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70236"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148214208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Self-Reported Sleep Duration, Death-Censored Graft Failure and Health-Related Quality of Life Among Kidney Transplant Recipients: Results From the KNOW-KT Study.","authors":"Hee-Yeon Jung, Yu Jin Seo, Kyu Ha Huh, Jae Berm Park, Myung-Gyu Kim, Kyung Pyo Kang, Seungyeup Han, Jang-Hee Cho, Sun-Hee Park, Chan-Duck Kim, Yong-Lim Kim, Jung-Hwa Ryu, Jaeseok Yang","doi":"10.1111/nep.70229","DOIUrl":"10.1111/nep.70229","url":null,"abstract":"<p><strong>Aim: </strong>Sleep duration is associated with cardiovascular events, mortality and rapidly declining kidney function in the general population. Less is known about its impact on transplant outcomes and health-related quality of life (HRQOL) among kidney transplant recipients (KTRs).</p><p><strong>Methods: </strong>This prospective multicenter longitudinal cohort study included 986 incident KTRs and investigated self-reported sleep duration at the time of kidney transplantation. Analyses were performed to examine associations between sleep duration and biopsy-proven acute rejection, death-censored graft failure, major cardiovascular events, all-cause mortality and HRQOL.</p><p><strong>Results: </strong>During a median follow-up period of 8 years, the death-censored graft failure rate was significantly higher among patients with sleep durations of ≤ 5 h (adjusted hazard ratio [aHR], 3.69; 95% confidence interval [CI], 1.42-9.57; p = 0.007), 6 h (aHR, 3.25; 95% CI, 1.34-7.87; p = 0.009), 8 h (aHR, 2.93; 95% CI, 1.22-7.01; p = 0.016) and ≥ 9 h (aHR, 3.58; 95% CI, 1.29-9.93; p = 0.014), compared to patients with a 7-h sleep duration. Sleep duration was not significantly associated with biopsy-proven acute rejection, major cardiovascular events or all-cause mortality. Multivariable linear regression demonstrated that shorter sleep duration (≤ 5 h) was associated with lower HRQOL, indicated by decreases in the physical component summary score (β, -4.51; 95% CI, -8.75 to -0.26; p = 0.038) and mental component summary score (β, -5.47; 95% CI, -10.29 to -0.65; p = 0.026), relative to patients with a 7-h sleep duration.</p><p><strong>Conclusion: </strong>Compared to a 7-h sleep duration, both shorter and longer sleep durations were associated with a significantly higher risk of death-censored graft failure among incident KTRs. Additionally, short sleep duration was significantly correlated with impaired HRQOL.</p><p><strong>Trial registration: </strong>NCT02042963; clinicaltrials.gov identifier.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70229"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Finerenone Attenuates Peritoneal Fibrosis by Restoring Autophagy Flux.","authors":"Feng Gao, YaoRong Wang, JingFang Han, XiaoLi Chen","doi":"10.1111/nep.70222","DOIUrl":"10.1111/nep.70222","url":null,"abstract":"<p><strong>Aim: </strong>Peritoneal fibrosis (PF) is a progressive complication of long-term peritoneal dialysis, driven primarily by high-glucose-induced mesothelial injury, epithelial-mesenchymal transition, and chronic inflammation. Emerging evidence implicates autophagy dysfunction as a pivotal contributor to PF progression. Finerenone, a novel non-steroidal mineralocorticoid receptor antagonist, has shown potent anti-fibrotic and anti-inflammatory effects in cardiorenal diseases, yet its role in peritoneal fibrosis remains incompletely understood. This study aimed to investigate whether Finerenone alleviates PF by regulating autophagy activity in peritoneal mesothelial cells.</p><p><strong>Methods: </strong>A mouse model of peritoneal fibrosis was established by daily intraperitoneal injection of 4.25% glucose-based peritoneal dialysis solution for 28 days. Finerenone (10 mg/kg) was administered orally concomitantly with dialysis fluid for 28 days. In vitro, human peritoneal mesothelial cells (HPMCs) were stimulated with TGF-β1 (2 ng/mL, 36 h) to induce fibrotic transformation. Cellular morphology, collagen deposition (Masson staining), and fibrosis markers (α-SMA, Fibronectin, Collagen I, and E-cadherin) were assessed by immunohistochemistry, immunofluorescence, and Western blot. Autophagy activity was evaluated by LC3-II/LC3-I ratio, p62 degradation, Beclin-1 and Atg5 expression, and chloroquine (CQ) co-treatment. Finally, Atg5 was silenced using siRNA to confirm its role in Finerenone-induced autophagy.</p><p><strong>Results: </strong>Finerenone markedly attenuated peritoneal thickening and collagen accumulation in vivo and suppressed TGF-β1-induced fibrotic phenotype in HPMCs. Finerenone decreased α-SMA, Fibronectin, and Collagen I expression while restoring E-cadherin levels. Mechanistically, Finerenone reversed TGF-β1-induced autophagy blockade, as evidenced by increased LC3-II/LC3-I and Beclin-1, upregulated Atg5, and decreased p62 accumulation, indicating enhanced autophagic flux. The autophagy inhibitor CQ abolished these protective effects, leading to LC3-II and p62 accumulation. Moreover, Atg5 knockdown counteracted Finerenone-mediated suppression of fibrosis-related proteins, confirming that Finerenone's anti-fibrotic effects depend on Atg5-mediated autophagy activation. Finerenone also reduced pro-inflammatory cytokines (TGF-β1, IL-6, and IL-1β), suggesting that autophagy restoration alleviates inflammation in parallel.</p><p><strong>Conclusion: </strong>Finerenone alleviates peritoneal fibrosis, at least in part, by restoring Atg5-mediated autophagic flux and suppressing inflammation in peritoneal mesothelial cells. These findings provide mechanistic insight into its antifibrotic effects and support autophagy modulation as a potential therapeutic strategy for peritoneal dialysis-associated complications.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70222"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contrast-Associated Acute Kidney Injury: Balancing Kidney Risk and Access to Essential Imaging.","authors":"Kody Shaw, Grace Chia, Rob Walker","doi":"10.1111/nep.70233","DOIUrl":"10.1111/nep.70233","url":null,"abstract":"<p><p>Iodinated contrast media are central to modern medicine, but have historically been associated with contrast-induced nephropathy (CIN), prompting widespread caution when imaging patients with kidney disease. This has led to delays, precautionary measures and avoidance of clinically indicated imaging. Contemporary evidence suggests that the risk of clinically meaningful kidney injury attributable to modern contrast agents has been overstated. We conducted a structured narrative review of the literature examining iodinated contrast media and kidney injury. Searches of PubMed/MEDLINE, Embase, Scopus and Google Scholar were performed in January 2026. Evidence was synthesised to evaluate the incidence, pathogenesis, clinical outcomes and prevention of contrast-associated acute kidney injury. Early reports of CIN were largely based on uncontrolled observational studies that attributed post-contrast creatinine rises to nephrotoxicity without appropriate comparator groups. Contemporary controlled studies demonstrate no independent association between intravenous contrast and clinically meaningful outcomes such as dialysis, chronic kidney disease progression or mortality. Experimental models show plausible mechanisms of injury but often rely on conditions not representative of routine practice. Biomarker studies highlight discordance between functional and structural kidney injury. Preventive strategies, including prophylactic hydration, have not demonstrated benefit in high-quality trials. Overall, clinically significant kidney injury attributable to modern iodinated contrast media appears uncommon. Excessive caution may delay or prevent necessary diagnostic and therapeutic procedures. A balanced, evidence-based approach prioritising timely imaging while addressing modifiable risk factors may improve patient outcomes and reduce barriers to care. The evidence synthesised in this review informs updated national guidance on contrast use in Aotearoa New Zealand.</p>","PeriodicalId":520716,"journal":{"name":"Nephrology (Carlton, Vic.)","volume":"31 6","pages":"e70233"},"PeriodicalIF":1.9,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148059274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}